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Rheumatology Flashcards

1
Q

RA definition

A

Chronic, systemic inflammatory disorder characterised by inflammatory polyarthritis

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2
Q

RA aetiology/risk factors

A

Genetics
Family history - 3 fold increase if first-degree relative affected
Demographics - middle-aged females of North American & Western European
Lower socioeconomic status
Smoking
Infections
Occupational exposures

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3
Q

RA pathophysiology

A

Trigger event
Development of self-citrullination (alteration of +ve arginine into neutral citrulline)
Immune system reacts to citrullinated proteins - development of anti-CCP antibodies
Multiple components of the innate and adaptive immune system are activated
Causes infiltration of synovial joints with immune cells and subsequent pro-inflammatory response

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4
Q

RA symptoms

A

Polyarthropathy - MCPJ, wrist joint, PIPJ, knee joint, MTPJ
Joint pain
Joint swelling
Joint stiffness - early morning stiffness lasting > 1 hour
Systemic - myalgia, fatigue, low-grade fever, weight loss and low mood

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5
Q

RA signs

A

Joint swelling
Pain on palpation of joints
Reduced range of movement
Difficulty with fine motor tasks
Muscle atrophy

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6
Q

RA classical signs

A

Boutonniere deformity - flexion at PIPJ with hyperextension of DIPJ
Swan-neck deformity - hyperextension at PIPJ with flexion of DIPJ
Ulnar deviation at MCPs - subluxation of MCPJ with deviation of the fingers towards the ulnar bone
Z-deformity at wrist - hyperextension of IPJ of thumb with carpal bone rotation and radial deviation & ulnar deviation at MCPJ
Hammer toes - compensatory flexion of the toes

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7
Q

RA extra-articular manifestations

A

Ocular - keratoconjunctivitis sicca, episcleritis, scleritis
Oral - xerostoma, oral ulcers
Pulmonary - ILD, serositis, costochondritis
Cardiac - pericarditis, myocarditis, non-infective endocarditis, increased risk of IHD
Renal - glomerulonephritis
Neurological - peripheral neuropathy, entrapment mononeuropathies, cervical myelopathy
Haemotological - neutropenia, thrombocytopaenia/thrombocytosis, haematological malignancies, anaemia of chronic disease
Dermatological - rheumatoid nodules, vasculitis skin rash, pyoderma gangrenosum

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8
Q

RA investigations

A

Bloods - FBC, U&E, bone profile, vit D, LFT, CRP, ESR, autoimmune screen
Rheumatoid factor - IgM autoantibody that reacts against Fc portion of IgG (seen in 60-70% of RA patients)
Anti-CCP - 80% of patients with RA
X-rays - hands and feet
-Soft tissue swelling
-Periarticular osteopaenia
-Joint space narrowing
-Boney erosions
Ultrasound
MRI

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9
Q

RA diagnostic criteria

A

Referred to a rheumatologist for further assessment
ACR/EULAR is a score-based system that looks at 4 domains:
-Joint involvement
-Serology tests (seropositive/seronegative)
-Acute phase reactants (markers of inflammation)
-Patient reported symptoms
Score applied when at least one joint has definitive synovitis & not better explained by another disease
Definite diagnosis = patients scores 6/10 or has erosive boney changes classical of RA

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10
Q

RA general management

A

General care - access to specialist services, holistic monitoring, screening for extra-articular manifestations
Symptom control - NSAIDs, specialist OT, PT

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11
Q

RA pharmacological management

A

Initial therapy - DMARD first line (eg. methotrexate, leflunomide or sulfasalazine)
-In combination with bridging steroid therapy (2-3 months), which allows time for DMARD to take effect
-Methotrexate
-Leflunomide
-Sulfasalazine
-Hydroxychloroquine
Failure to response - combined DMARD ‘step-up’ therapy
Biologic therapy - inadequate response to DMARD & ongoing active disease
-TNF inhibitor - adalimumab, golimumab, infliximab
-Rituximab - anti-CD20 antibody
-Tocilizumab - anti-IL-6 antibody
Managing flares - acute courses of corticosteroids (eg. prednisolone)
Step-down strategy - reducing/stopping therapy in patient who have maintained remission for > 1 year without corticosteroids

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12
Q

RA complications

A

Accelerated atherosclerosis
Associated IHD
Medication side-effects (osteoporosis, higher risk of malignancy)

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13
Q

SLE pathophysiology

A

Exposure of the immune system to blebs from apoptotic cells
The blebs (feature self-antigens) are not efficiently removed and are carried to lymphoid tissue
Immune response is raised when these are taken up by antigen-presenting cells and presented to T-lymphocytes resulting in B-lymphocyte activation & autoantibody production
Failure to inactivate lymphocytes -> circulating autoantibodies & immune-mediated damage to ones own cells

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14
Q

SLE symptoms

A

Fatigue
Malaise
Weight loss
Fever
Myalgia

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15
Q

SLE signs

A

Symmetrical small joint polyarticular arthritis
Malar rash (erythematous rash that lies on the cheeks and across the bridge of the nose)
Photosensitivity & alopecia

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16
Q

SLE extra-articular manifestations

A

Kidneys - nephritis
Lungs - pleurisy, pneumonitis, pleural effusions, pulmonary fibrosis
CVS - pericarditis, myocarditis, heart block
Neuropsychiatric - seizures, ataxia and psychosis
Sjogren’s syndrome
Anaemia of chronic disease

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17
Q

SLE investigations

A

Bedside - vital signs, blood sugar, ECG
Bloods - FBC, U&Es, clotting, LFTs, ESR/CRP, CK, vitamin D3, TFTs
Immunology:
-Antinuclear antibody - positive in about 95% patients with SLE
C3/C4 - low levels seen
-Anti-dsDNA and anti-Smith antibodies - specific for SLE
-Antiphospholipid antibodies - ordered particularly for those who have past history of miscarriages or venous thromboembolism
-Anti-RO/LA and anti-RNP antibodies - poor sensitivity
-Direct coombs test - evidence of haemolytic anaemia
-Immunoglobulins
Urine - urinalysis, random protein:creatinine ratio/24-hr urine collection for protein
Imaging - CXR, MSK XR, renal USS, CT chest, CT/MRI brain, ECHO
Biopsy
Skin - immunofluorescence shows immune deposits at the dermal-epidermal boundary
Kidney - highly sensitive and specific for lupus nephritis

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18
Q

SLE diagnostic criteria

A

EULAR/ACR (2019) - positive ANA is required, then there are ten criteria (clinical and immunological) with patient said to have SLE if they score 10/more points

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19
Q

SLE management

A

Active and healthy lifestyles, regular reviews and optimisation of other medical conditions, use of SPF advised
Induction therapy - aimed at halting disease progression and inducing remission
-Prednisolone and hydroxychloroquine used with combination of others depending on severity (eg. azathioprine, mycophenolate)
Maintenance - preventing relapse, once stable remission is achieved then immunosuppressants can be stopped, with only hydroxychloroquine continuing

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20
Q

SLE complications

A

Thrombosis
Infections
CVS disease
Treatment complications

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21
Q

Ankylosing spondylitis

A

Chronic, multi-system inflammatory disorder characterised by inflammation of the sacroiliac joints & axial skeleton

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22
Q

Ankylosing spondylitis pathophysiology

A

Early sacroiliac joint involvement leading to inflammatory back pain
Followed by involvement of the spine -> initial inflammation at the junction between the vertebrae and intervertebral discs
Annulus fibrosis undergoes ossification & forms syndesmophytes
These may bridge together across multiple vertebrae leading to the classic ‘bamboo’ spine that significantly reduces spinal mobility

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23
Q

Ankylosing spondylitis symptoms

A

Back pain - worse with inactivity, improves with exercise
Neck pain
Alternating buttock pain
Morning stiffness
Fatigue
Arthritis

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24
Q

Ankylosing spondylitis signs

A

Enthesitis - inflammation at the insertion of tendons and ligaments
Positive Schober test - assesses decreases in lumbar spine flexion
Spinal deformity

25
Ankylosing spondylitis extra-articular manifestations
Aortitis Anterior uveitis AV block Atlanto-axial instability Apical lung fibrosis Amyloidosis IgA nephropathy
26
Ankylosing spondylitis investigations
Bloods - routine, inflammatory markers, HLA-B27 (negative test does not exclude the diagnosis) X-rays - spinal/pelvic x-rays Advanced disease: -Dagger sign - ossification of the supraspinous and interspinous ligaments leading to central radiodense line running up the spine -Bamboo sign - vertebral body fusion by marginal syndesmophytes & squaring of vertebral bodies, impression of a continuous lateral spinal border MRI
27
Ankylosing spondylitis diagnostic criteria
Patient < 45 years old with a 3 month history of lower back pain should be referred to rheumatologist for assessment of SpA if > 4 of the following criteria are met: -Onset < 35 years old -Waking during second half of night -Buttock pain -Improves with exercise -Improves with NSAIDs -First-degree relative with SpA -Current/past arthritis -Current/past enthesitis -Current/past psoriasis 1984 modified new york criteria Clinical criteria -Low back pain >/= 3 months, improved by exercise and not relieved by rest -Limitation of lumbar spine in sagittal and frontal planes -Limitation of chest expansion Radiological criteria -Bilateral grade 2-4 sacroilitis OR -Unilateral grade 3-4 sacroilitis Diagnosis Definite - radiological criteria present & at least one clinical criterion Probable - either radiological criterion or 3 clinical criteria present alone
28
Ankylosing spondylitis management
Use of non-pharmacological treatments and NSAIDs Patients with severe disease/non-response to initial therapy - DMARDs, biologics
29
Ankylosing spondylitis complications
Spinal fusion Spinal fractures Osteoporosis Restrictive lung disease Spinal cord injury Cardiac disease - valvular disease, HF, arrhythmias
30
Gout
Crystal arthropathy resulting from excess levels of uric acid leading to precipitation in joints and other tissue
31
Gout aetiology
1) Purine overproduction - occurs when there is increased cell turnover/lysis of cells leading to release of purines and breakdown to uric acid -Myelo- or lymphoproliferative disorders -Psoriasis -Use of chemotherapy agents 2) Increased purine intake -Seafood -Red meat -Alcohol -Fructose-rich beverages 3) Decreased uric acid secretion -Diuretics -AKI -CKD -ACEi -Diabetes mellitus
32
Gout pathophysiology
Monosodium urate crystals precipitate in peripheral joints - less soluble at low temperatures Deposition of crystals within joints and soft-tissue may occur asymptomatically (chronic gout) or during acute attacks, crystals trigger an acute inflammatory reaction leading to acutely painful swollen joints
33
Gout symptoms and signs
Symptoms -Joint pain -Joint swelling Signs -Erythema -Tophi -Degenerative arthropathy
34
Gout investigations
Bloods - serum uric acid -4-6 weeks following an acute attack Joint aspiration - gold standard investigation -Sent for crystal microscopy, microscopy, cultures & sensitives -Needle-shaped crystals, negatively birefringent of polarised light, monosodium urate crystals Plain radiographs -Joint space is maintained -Lytic lesions in the bone -Punched out erosions -Erosions can have sclerotic borders with overhanging edges
35
Gout management
Acute management -General advice - rest, ice & elevation -First-line therapy - offer NSAIDs or oral colchicine --Co-prescribe a PPI for gastric protection if giving an NSAID -Second-line therapy - short course of oral steroids/intra-articular injection of steroids Prevention -First-line therapy - allopurinol --Care must be taken in renal impairment -Second-line therapy - febuxostat --Must have LFTs prior & commencing febuxostat
36
Fibromyalgia
A syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites
37
Fibromyalgia symptoms
Chronic pain Lethargy Cognitive impairment Sleep disturbance Headaches Dizziness
38
Fibromyalgia diagnostic criteria
ACR classification criteria -Lists 9 pairs of tender points on the body -If patient is tender in at least 11 of these 18 points -> makes diagnosis more likely
39
Fibromyalgia management
Difficult and needs to be tailored to the individual patient Explanation Aerobic exercise CBT Medication - pregabalin, duloxetine & amitriptyline
40
Osteomalacia
Describes softening of the bones secondary to low vitamin D levels that in turn lead to decreased bone mineral content
41
Osteomalacia aetiology
Vitamin D deficiency CKD Coeliac disease Liver disease Cirrhosis
42
Osteomalacia pathophysiology
Inadequate vitamin D leads to lack of calcium and phosphate in the blood Low levels result in defective bone mineralisation Low calcium causes a secondary hyperparathyroidism - parathyroid gland tries to raise calcium level by secreting PTH -> increased reabsorption from bones -> further problems with bone mineralisation
43
Osteomalacia symptoms
Fatigue Bone pain Muscle weakness Muscle aches Pathological/abnormal fractures
44
Osteomalacia investigations
Serum 25-hydroxyvitamin D -<25 nmol/L - vitamin D deficiency -25 - 50 nmol/L - vitamin D insufficiency -75 nmol/L or above is optimal Bloods - calcium, phosphate, ALP, PTH X-rays -Osteopenia (more radiolucent bones) DEXA scan -Low bone mineral density
45
Osteomalacia management
Supplementary vitamin D (cholecalciferol) -50,000 IU once weekly for 6 weeks -20,000 IU twice weekly for 7 weeks -4000 IU daily for 10 weeks Maintenance supplementary dose of 800 IU should be continued for life after initial treatment -Patients with vit D insufficiency can be started on this
46
Osteoporosis
Characterised by low bone mass and micro-architectural deterioration of bone with resulting fragility and fracture risk Defined as a bone mineral density of 2.5 SDs below the mean peak mass
47
Osteoporosis pathophysiology
Imbalance of bone breakdown & bone formation -As we age, the activity of osteoclasts increase & not matched by osteoblasts --Bone mass decreases -Following menopause, oestrogen deficiency leads to an increased rate of age-related bone loss --Affects cancellous and cortical bone -Glucocorticoids - cause increased bone turnover --Prolonged use can result in a reduced turnover state though even here synthesis is affected more leading to a loss of bone mass
48
Osteoporosis fracture risk
Low BMD is associated with a significantly increased risk of fracture Use of FRAX and QFracture tools are advised to help determine who to investigate further with a DXA Can be used to calculate the risk of fracture over a 10 year period
49
Osteoporosis investigations
Dual-energy X-ray absorptiometry scans are used to assess BMD -Clinicians may proceed straight to DXA in patients over the age of 50 who have history of fragility fracture/arranged for those younger than 40 with a major risk factor -Utilises X-rays to assess the density of bones (commonly the hip and spine) --Normal - T-score > -1 --Osteopenia - T of -1 to -2.5 --Osteoporosis - T score of
50
Osteoporosis management
Oral bisphosphonates are first-line -Alendronate - commonly used & is licensed in postmenopausal osteoporosis & osteoporosis in men --Must be taken in the morning with a glass of water (after fasting overnight)/at least 30 minutes prior to any food or drink --After taking it the patient must stay upright for 30 mins -Zoledronic acid - may be used in those not tolerating oral preparations IV injection once a year Denosumab - given via s.c. every 6 months Raloxifene - SORM (may be used in postmenopausal osteoporosis) HRT
51
Polymyalgia rheumatica
Systemic inflammatory disease which is characterised by shoulder and hip girdle pain
52
PR symptoms
Bilateral shoulder and/or hip girdle pain Stiffness and upper limb tenderness - particularly in the mornings Systemic - low-grade fever, fatigue, weight loss Low mood Peripheral - arthritis, swelling and carpal tunnel syndrome
53
PR signs
Reduced range of movement Inability to abduct shoulders past 90 degrees Synovitis and swelling Muscles atrophy
54
PR investigations
Bloods - FBC, U&E, LFT, ESR/CRP, bone profile, TFT, CK, RF, HbA1c Specialist bloods - myeloma screen, autoimmune screen Imaging - CXR, shoulder XR, MSK US, MRI
55
PR diagnostic criteria
Should be considered if: -Age - 50 years or older -Typical symptoms - bilateral, symmetrical shoulder and/or hip girdle pain associated with stiffness -Duration - > 2 weeks and lasting > 45 mins at a time -Elevated ESR/CRP -Rapid resolution of symptoms with corticosteroids
56
PR management
Corticosteroids - oral prednisolone 15mg daily -Patients should be reviewed in one week to assess the response to treatment -Should be reduced once symptoms are fully controlled (usually after a period of 3-4 weeks) -May be over a long period due to risk of relapse/stopping too early -Need bone protection, gastric protection and BM monitoring Rheumatology referral - atypical symptoms, problems with steroids GCA screening and management - high dose corticosteroids
57
PR complications
Steroid related (give steroid emergency card) -Hyperglycaemia -Mood changes -Insomnia -GI bleeding -Immunosuppression
58
PR follow-up
Should be assessed after one week of treatment to assess for a response Three-monthly within the first year

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